Role of K+ Channels in Frequency Regulation of Spontaneous Action Potentials in Rat Pituitary GH3 Cells

2003 ◽  
Vol 78 (5) ◽  
pp. 260-269 ◽  
Author(s):  
Suk-Ho Lee ◽  
Eun Hae Lee ◽  
Shin Young Ryu ◽  
Hyewhon Rhim ◽  
Hye-Jung Baek ◽  
...  
Keyword(s):  
Action Potentials ◽  
Frequency Regulation ◽  
Rat Pituitary ◽  
Spontaneous Action ◽  
Spontaneous Action Potentials

scholarly journals SK Current, Expressed During the Development and Regeneration of Chick Hair Cells, Contributes to the Patterning of Spontaneous Action Potentials

2022 ◽  
Vol 15 ◽  
Author(s):  
Snezana Levic
Keyword(s):  
Electrical Activity ◽  
Hair Cells ◽  
Action Potentials ◽  
Functional Expression ◽  
Basilar Papilla ◽  
Spontaneous Electrical Activity ◽  
Intracellular Ca ◽  
Spontaneous Action ◽  
Spontaneous Action Potentials

Chick hair cells display calcium (Ca2+)-sensitive spontaneous action potentials during development and regeneration. The role of this activity is unclear but thought to be involved in establishing proper synaptic connections and tonotopic maps, both of which are instrumental to normal hearing. Using an electrophysiological approach, this work investigated the functional expression of Ca2+-sensitive potassium [IK(Ca)] currents and their role in spontaneous electrical activity in the developing and regenerating hair cells (HCs) in the chick basilar papilla. The main IK(Ca) in developing and regenerating chick HCs is an SK current, based on its sensitivity to apamin. Analysis of the functional expression of SK current showed that most dramatic changes occurred between E8 and E16. Specifically, there is a developmental downregulation of the SK current after E16. The SK current gating was very sensitive to the availability of intracellular Ca2+ but showed very little sensitivity to T-type voltage-gated Ca2+ channels, which are one of the hallmarks of developing and regenerating hair cells. Additionally, apamin reduced the frequency of spontaneous electrical activity in HCs, suggesting that SK current participates in patterning the spontaneous electrical activity of HCs.

Spontaneous electrical rhythmicity and the role of the sarcoplasmic reticulum in the excitability of guinea pig gallbladder smooth muscle cells

2006 ◽  
Vol 290 (4) ◽  
pp. G655-G664 ◽  
Author(s):  
Onesmo B. Balemba ◽  
Matthew J. Salter ◽  
Thomas J. Heppner ◽  
Adrian D. Bonev ◽  
Mark T. Nelson ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Action Potentials ◽  
Cyclopiazonic Acid ◽  
Cellular Mechanisms ◽  
Voltage Dependent ◽  
Spontaneous Action ◽  
Potential Activity ◽  
Spontaneous Action Potentials

Spontaneous action potentials and Ca2+ transients were investigated in intact gallbladder preparations to determine how electrical events propagate and the cellular mechanisms that modulate these events. Rhythmic phasic contractions were preceded by Ca2+ flashes that were either focal (limited to one or a few bundles), multifocal (occurring asynchronously in several bundles), or global (simultaneous flashes throughout the field). Ca2+ flashes and action potentials were abolished by inhibiting sarcoplasmic reticulum (SR) Ca2+ release via inositol (1,4,5)-trisphosphate [Ins(1,4,5)P3] channels with 2-aminoethoxydiphenyl borate and xestospongin C or by inhibiting voltage-dependent Ca2+ channels (VDCCs) with nifedipine or diltiazem or nisoldipine. Inhibiting ryanodine channels with ryanodine caused multiple spikes superimposed upon plateaus of action potentials and extended quiescent periods. Depletion of SR Ca2+ stores with thapsigargin or cyclopiazonic acid increased the frequency and duration of Ca2+ flashes and action potentials. Acetylcholine, carbachol, or cholecystokinin increased synchronized and increased the frequency of Ca2+ flashes and action potentials. The phospholipase C (PLC) inhibitor U-73122 did not affect Ca2+ flash or action potential activity but inhibited the excitatory effects of acetylcholine on these events. These results indicate that Ca2+ flashes correspond to action potentials and that rhythmic excitation in the gallbladder is multifocal among gallbladder smooth muscle bundles and can be synchronized by excitatory agonists. These events do not depend on PLC activation, but agonist stimulation involves activation of PLC. Generation of these events depends on Ca2+ entry via VDCCs and on Ca2+ mobilization from the SR via Ins(1,4,5)P3 channels.

Regional differences in the role of the Ca2+ and Na+ currents in pacemaker activity in the sinoatrial node

1997 ◽  
Vol 272 (6) ◽  
pp. H2793-H2806 ◽  
Author(s):  
I. Kodama ◽  
M. R. Nikmaram ◽  
M. R. Boyett ◽  
R. Suzuki ◽  
H. Honjo ◽  
...  
Keyword(s):  
Action Potentials ◽  
Regional Differences ◽  
Sinoatrial Node ◽  
Pacemaker Activity ◽  
Na Current ◽  
Na Currents ◽  
Spontaneous Action ◽  
Spontaneous Action Potentials ◽  
Rabbit Sinoatrial Node

The effect of block of the L-type Ca2+ current by 2 microM nifedipine and of the Na+ current by 20 microM tetrodotoxin on the center (normally the leading pacemaker site) and periphery (latent pacemaker tissue) of the rabbit sinoatrial node was investigated. Spontaneous action potentials were recorded with microelectrodes from either an isolated right atrium containing the whole node or small balls of tissue (approximately 0.3-0.4 mm in diameter) from different regions of the node. Nifedipine abolished the action potential in the center, but not usually in the periphery, in both the intact sinoatrial node and the small balls. Tetrodotoxin had no effect, on electrical activity in small balls from the center, but it decreased the takeoff potential and upstroke velocity and slowed the spontaneous activity (by 49 +/- 10%; n = 11) in small balls from the periphery. It is concluded that whereas the L-type Ca2- current plays an obligatory role in pacemaking in the center, the Na+ current plays a major role in pacemaking in the periphery.

Response of Ca(2+)-loaded, depolarized guinea pig myocytes to critically timed premature stimulations

1996 ◽  
Vol 270 (2) ◽  
pp. H447-H465
Author(s):  
C. Nordin
Keyword(s):  
Membrane Potential ◽  
Guinea Pig ◽  
Action Potentials ◽  
Low Dose ◽  
Tyrode Solution ◽  
Coupling Interval ◽  
Spontaneous Action ◽  
Experimental Response ◽  
Spontaneous Action Potentials

Single premature stimulations during trains of nondriven action potentials induced by depolarization normally cause a transient hyperpolarization of diastolic membrane potential before the subsequent spontaneous upstroke. However, rare, marked transient depolarizations have also been reported. This paper presents experimental data and computer simulations that characterize transient depolarization following premature stimulations and investigate the role of intracellular [Ca2+] in generating this unusual response. In isolated guinea pig myocytes, transient depolarizations (range 4-58 mV) consistently occurred following stimulations 100-160 ms after the upstroke of spontaneous action potentials during exposure to K(+)-free Tyrode solution, which raises intracellular [Ca2+]. In contrast, no transient depolarizations developed when stimulations were delivered during injection of constant inward current or brief exposure to very low dose of Ba2+ (250-500 microM). The experimental response to K(+)-free Tyrode solution was reproduced by a computer model of the transmembrane current and intracellular Ca2+ flux of an isolated guinea pig ventricular myocyte (24) following reduction of extracellular [K+] below 1 mM. Transient depolarization was generated primarily by Na/Ca exchange. Simulations using only those equations governing intracellular Ca2+ cycling revealed that bursts of Ca2+ into the myoplasm after Ca2+ loading caused a transient increase in trough myoplasmic [Ca2+] when the coupling interval following the upstroke of a myoplasmic [Ca2+] oscillation was nearly identical to those coupling intervals that caused pacing-induced transient depolarization of membrane potential after the upstroke of an action potential. These results suggest that transient depolarizations following nondriven action potentials arise from critically timed, stimulus-induced perturbation of intracellular [Ca2+] oscillations associated with Ca2+ overload. Simulations using a multicellular model suggest that critically timed premature stimulations can initiate trains of depolarized, nondriven action potentials in otherwise quiescent, Ca(2+)-overloaded heterogeneous syncytia by a similar mechanism.

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